doi: 10.1001/archinte.1984.00350220016001pmid: N/A
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.
doi: 10.1001/archinte.1984.00350220021002pmid: N/A
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.
doi: 10.1001/archinte.1984.00350220025003pmid: N/A
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.
doi: 10.1001/archinte.1984.00350220025004pmid: N/A
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.
doi: 10.1001/archinte.1984.00350220029006pmid: N/A
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract This slender volume starts out with the best of intentions. At the present time, there is no written body of knowledge under one cover that pertains to occupational diseases caused by fungi. Therefore, the aim of the book is laudible. Unfortunately, closer reading of the book will show that relatively little is known about the occupational risks of fungal diseases. This multiauthored text, most of whose authors are well-known authorities in mycology, have done yeoman's duty in attempting to bring together the markedly diffused and dispersed body of knowledge under one cover. Regrettably, this attempt further underscores our woeful ignorance in the role of fungi in occupational diseases. The format of the book is fairly standard, with single chapters being devoted to the major fungi. It is in the first chapters, dealing with the pathogenic fungi, where the sparsity of known material is so disturbing. Under the heading of occupational
doi: 10.1001/archinte.1984.00350220029005pmid: N/A
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract This volume is a much revised and updated edition of the text these authors first published seven years ago. The book is subtitled A Pathophysiological Approach, and in fact, its uniqueness and value lie in the authors' adherence to this approach. The first half of the book is a review, in some detail, of normal pulmonary physiology. The diagrams and tables in this section are excellent. The chapters vary somewhat in quality. The chapter on lung mechanics is very complete and is a good reference source for the physiology student. The chapters on lung defenses and respiratory control are considerably more sketchy but adequate for the beginning medical student. The real forte of this book is the second section on pathophysiology. The chapters on lung function testing are among the finest I have read on the subject. The explanations are excellent and the practical approach allows for a reasoned evaluation
doi: 10.1001/archinte.1984.00350220029007pmid: N/A
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract Pleural effusions are common in clinical medicine. Patients with pleural effusion may be seen by the internist (cardiologist, congestive heart failure; gastroenterologist, pancreatitis) or surgeon (cardiothoracic surgeon, post— cardiac injury syndrome; gynecologist, Meigs' syndrome). Indeed, pleural effusions are a mirror of systemic disease. Dr Light has written this book on pleural disease based on years of clinical observation and research. There are 24 chapters in this book, three chapters devoted to anatomy of the pleura, physiology of the pleural space, and radiology of pleural disease. An additional two chapters concentrate on clinical manifestations of pleural disease and the usefulness of pleural fluid analysis and the general approach to a patient with a pleural effusion. The two concluding chapters discuss thoracentesis, pleural biopsy, and chest tubes. In between there are chapters on the specific etiologies of pleural effusions covering the spectrum from congestive heart failure to malignant pleural effusions to chylothorax.
doi: 10.1001/archinte.1984.00350220049008pmid: N/A
Abstract The founding fathers were not referring to the medical literature when they proclaimed that certain facts were obviously true and required only brief consideration to recognize their veracity. Unfortunately, many academic and practicing physicians seem to have taken this quotation to heart with respect to their understanding of a variety of medical paradigms. One of the most frequently cited and fervently held concepts is the association between mitral valve prolapse (MVP) and arrhythmias. The rare occurrence of sudden cardiac death in patients with MVP has raised a frightening spectre before these patients, the vast majority of whom will have no sequelae whatsoever.1-5 In this issue of the Archives, Kramer and his associates question the previously "self-evident" tenet that patients with MVP are remarkably prone to both supraventricular and ventricular arrhythmias.6 Similar "heretical" data has recently been published by Savage et al.7 See also p 2360. Since MVP References 1. Chesler E, King RA, Edwards JE: The myxomatous valve and sudden death. Circulation 1983;67:632-639.Crossref 2. Jeresaty RM: Mitral valve prolapse-click syndrome: Etiology, clinical findings, and therapy. J Cardiovasc Med 1978;3:597-613. 3. Shappell SD, Marshall CE: Ballooning posterior leaflet syndrome: Syncope and sudden death. Arch Intern Med 1975;135: 664-667.Crossref 4. Ritchie JL, Hammermeister KE, Kennedy JW: Refractory ventricular tachycardia and fibrillation in a patient with the prolapsing mitral leaflet syndrome: Successful control with overdrive pacing. Am J Cardiol 1976;37:314-318.Crossref 5. Wei JY, Bulkley BH, Schaeffer AH, et al: Mitral valve prolapse syndrome and recurrent ventricular tachyarrhythmias: A malignant variant refractory to conventional drug therapy. Ann Intern Med 1978;89:6-9.Crossref 6. Kramer HM, Kligfield P, Devereux RB, et al: Arrhythmias in mitral valve prolapse: Effect of selection bias. Arch Intern Med 1984;144:2360-2364.Crossref 7. Savage DD, Levy DL, Garrison RJ, et al: Mitral valve prolapse in the general population: III. Dysrhythmias: The Framingham study. Am Heart J 1983;106:582-586.Crossref 8. Morady F, Shen E, Bhandari A, et al: Programmed ventricular stimulation in mitral valve prolapse: Analysis of 36 patients. Am J Cardiol 1984;53:135-138.Crossref 9. Kolibash AJ, Bush CA, Fontana MB, et al: Mitral valve prolapse: Analysis of 62 patients aged 60 years and older. Am J Cardiol 1983;52:534-539.Crossref 10. DeMaria AN, Amsterdam EA, Vismara LA, et al: Arrhythmias in the mitral valve prolapse syndrome: Prevalence, nature and frequency. Ann Intern Med 1976;84:656-660.Crossref 11. Winkle RA, Lopes MG, Fitzgerald JW, et al: Arrhythmias in patients with mitral valve prolapse. Circulation 1975;52:73-81.Crossref 12. Josephson ME, Horowitz LN, Kastor JA: Paroxysmal supraventricular tachycardia in patients with mitral valve prolapse. Circulation 1978;57:111-115.Crossref 13. Sloman G, Wong M, Walker J: Arrhythmias on exercise in patients with abnormalities of the posterior leaflet of the mitral valve. Am Heart J 1972;83:313-317.Crossref 14. Kostis JB, McCrone K, Moreyra AE, et al: Premature ventricular complexes in the absence of identifiable heart disease. Circulation 1981;63:1351-1356.Crossref 15. Brodsky M, Wu D, Denes P, et al: Arrhythmias documented by 24-hour continuous electrocardiographic monitoring in 50 male medical students without apparent heart disease. Am J Cardiol 1977;39:390-395.Crossref 16. Sobotka PA, Mayer JH, Bauernfeind RA, et al: Arrhythmias documented by 24-hour continuous ambulatory electrocardiographic monitoring in young women without apparent heart disease. Am Heart J 1981;101:753-758.Crossref 17. Camm AJ, Evans KE, Ward DE, et al: The rhythm of the heart in active elderly subjects. Am Heart J 1980;99:598-603.Crossref 18. Kavey RW, Sondheimer HM, Blackman MS: Detection of dysrhythmia in pediatrie patients with mitral valve prolapse. Circulation 1980;62:582-587.Crossref 19. Bisset GS, Schwartz DC, Meyer RA, et al: Clinical spectrum and long-term follow-up of isolated mitral valve prolapse in 199 children. Circulation 1980;62:423-429.Crossref
Frishman, William H.;Charlap, Shlomo
doi: 10.1001/archinte.1984.00350220051009pmid: N/A
Abstract Nifedipine is a calcium-channel antagonist having the property of selective inhibition of transmembrane flux of calcium in excitable tissues.1 Its ability to block calcium-mediated electromechanical coupling in contractile tissue produces arterial dilation in both the coronary and peripheral vascular beds and provides the clinical rationale for use of the drug in the management of myocardial ischemic syndromes. Because systemic vasodilation can be expected to reduce elevated arterial BP, interest has focused on the use of nifedipine in the medical management of systemic hypertension. A postulated involvement of calcium in the development of the increased vascular tone of hypertension, makes nifedipine, and the other calcium-channel antagonists, appear particularly attractive for use as vasodilators.2 See also p 2357. The effectiveness of nifedipine in the acute treatment of severe hypertension and hypertensive emergencies has been demonstrated in several studies,3-6 including the study by Haft and Litterer3 in this Archives References 1. Fleckenstein A: Specific pharmacology of calcium in myocardium, cardiac pacemakers, and vascular smooth muscle. Annu Rev Pharmacol Toxicol 1977;17:149-166.Crossref 2. Spivack C, Ocken S, Frishman WH: Calcium antagonists: Clinical use in the treatment of systemic hypertension. Drugs 1983;25:154-177.Crossref 3. Haft JI, Litterer WE III: Chewing nifedipine to rapidly treat hypertension. Arch Intern Med 1984;144:2357-2359.Crossref 4. Beer N, Gallegos I, Cohen A, et al: Efficacy of sublingual nifedipine in the acute treatment of systemic hypertension. Chest 1981;79:571-574.Crossref 5. Guazzi MD, Olivari MT, Polese A, et al: Nifedipine, a new antihypertensive with rapid action. Clin Pharmacol Ther 1977;22: 528-532. 6. Takekoshi N, Murakami E, Murakami H, et al: Treatment of severe hypertension and hypertensive emergency with nifedipine, a calcium antagonistic agent. Jpn Circ J 1981;45:852-860.Crossref 7. Frishman WH, Weinberg P, Peled HB, et al: Calcium-entry blockers for the treatment of severe hypertension and hypertensive crisis. Am J Med , in press. 8. Aoki K, Kondo S, Mochizuki A, et al: Antihypertensive effect of cardiovascular Ca2+-antagonist in hypertensive patients in the absence and presence of β-adrenergic blockade. Am Heart J 1978;96:218-226.Crossref 9. Pederson OL, Christensen CK, Mikkelsen E, et al: Relationship between antihypertensive effect and steady state plasma concentration of nifedipine given alone or in combination with a β-adrenoceptor blocking agent. Eur J Clin Pharmacol 1980;18: 287-293.Crossref 10. Husted SE, Kraemer H, Christensen CK, et al: Long-term therapy of arterial hypertension with nifedipine given alone or in combination with β-adrenoceptorptor blocking agent. Eur J Clin Pharmacol 1982;22:101-103.Crossref 11. Lederballe Pederson O: Calcium blockade in arterial hypertension. Review. Hypertension 1983;5( (suppl 2) ):74-79. 12. Gould BA, Mann S, Kieso H, et al: The 24-hour ambulatory blood pressure profile with verapamil. Circulation 1982;65:22-27.Crossref 13. Inouye IK, Massie BM, Benowitz N, et al: Antihypertensive therapy with diltiazem and comparison with hydrochlorothiazide. Am J Cardiol 1984;53:1588-1592.Crossref 14. Erne P, Boll IP, Bertel 0, et al: Factors influencing the hypotensive effects of calcium antagonists. Hypertension 1983; 5( (suppl 2) ):85-90.Crossref 15. Guazzi MD, Fiorentini C, Olivari MT, et al: Short- and long-term efficacy of a calcium antagonistic agent (nifedipine) combined with methyldopa in the treatment of severe hypertension. Circulation 1980;61:913-919.Crossref 16. Dean S, Kendall MJ: Nifedipine in the treatment of difficult hypertensives. Eur J Clin Pharmacol 1983;24:1-5.Crossref 17. Evans MG Jr Jr, Olanoff LS, urwitz et al: Use of nifedipine as an adjunct to current antihypertensive therapy. Arch Intern Med 1984;144:985-987.Crossref
doi: 10.1001/archinte.1984.00350220052010pmid: N/A
Abstract Selective renal wasting of magnesium and hypomagnesemia resulting from an impaired ability of the kidneys to conserve magnesium normally is not unusual during and after treatment with cisplatin.1 The reported incidence has varied from less than 50%1-3 to nearly 100%.4-6 Although initially there was no association between the dose of cisplatin administered and the incidence of this complication, recent reports stress magnesium wasting proportionate to cisplatin dosage, with the number of patients exhibiting hypomagnesemia increasing progressively as the chemotherapy cycles are repeated.5,6 Furthermore, renal wasting of magnesium may persist long after cisplatin therapy is discontinued.1 Other measures used to prevent cisplatin-induced nephrotoxic activity, such as vigorous hydration with saline, mannitol diuresis, and loop diuretics, have all been shown to augment urinary magnesium losses. Many highly myelosuppressive cytotoxic agents are now being used aggressively together with cisplatin in the management of certain See also p 2347. References 1. Schilsky RL, Anderson T: Hypomagnesemia and renal magnesium wasting in patients receiving cisplatin. Ann Intern Med 1979;90:929-931.Crossref 2. Anderson T, Javadpour N, Schilsky R, et al: Chemotherapy for testicular cancer: Current status of the National Cancer Institute combined modality trial. Cancer Treat Rep 1979;63: 1687-1692. 3. Ozols RF, Corden BJ, Jacob J, et al: High-dose cisplatin in hypertonic saline. Ann Intern Med 1984;100:19-24.Crossref 4. Buckley JE, Clark VL, Meyer TH, et al: Hypomagnesemia after cisplatin combination chemotherapy. Arch Intern Med 1984; 144:2347-2348.Crossref 5. Hayes FA, Green AA, Senzer N, et al: Tetany: A complication of cis-dichlorodiammineplatinum (II) therapy. Cancer Treat Rep 1979;63:547-548. 6. Fernandez Vega F, Ortega Suarez F, Pannizo A, et al: Hypomagnesemia: A usual manifestation of cisplatinum nephrotoxicity, abstracted. Kidney Int 1983;24:130. 7. Chernow B, Zaloga GP, Pock A, et al: Aminoglycoside-induced hypomagnesemia: A prospective study, abstracted. Clin Res 1982;30:863A. 8. Keating MJ, Sethi MR, Bodey GP, et al: Hypocalcemia with hypoparathyroidism and renal tubular dysfunction associated with aminoglycoside therapy. Cancer 1977;39:1410-1414.Crossref 9. Patel R, Savage A: Symptomatic hypomagnesemia associated with gentamycin therapy. Nephron 1979;23:50-52.Crossref 10. Bar RS, Wilson HE, Mazzaferri EL: Hypomagnesemic hypocalcemia secondary to renal magnesium wasting: A possible consequence of high-dose gentamycin therapy. Ann Intern Med 1975;82:646-649.Crossref 11. Burges AL, Birchall R: Nephrotoxicity of amphotericin B, with emphasis on changes in tubular function. Am J Med 1972;53:77-84.Crossref 12. Alberts DS, Serpick AA, Thompson WL: Hypocalcemia complicating acute leukemia. Med Pediatr Oncol 1975;1:289-295.Crossref 13. Freedman DB, Shannon M, Dandona P, et al: Hypoparathyroidism and hypocalcemia during treatment for acute leukemia. Br Med J 1982;284:700-702.Crossref 14. Flombaum C, Vanamee P, Isaacs M, et al: Complications of forced diuresis during cancer chemotherapy, abstracted. Proc Am Soc Clin Oncol 1984;3:106.
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